The proposed studies will determine the correlation between cerebrospinal fluid endorphins, pulmonary hemodynamics, platelet trapping and intrapulmonary vascular changes that occur following the induction of neurogenic pulmonary edema, lung trauma, and endotoxin shock. The role of pulmonary neural traffic in these pathologic processes will be assessed; the protective effect of an endorphin antagonist will be evaluated. the methodology includes assays for endorphin and for Beta thromboglobulin (a marker for platelet release factors), isotopically-tagged platelets and fibrinogen, and measurements of tissue plasminogen activator. As a corollary, casts of the pulmonary circulation will be made in each group of experiments. These studies have relevance to understanding the mechanism of the acute respiratory distress syndrome and the pulmonary pathophysiology associated with shock, sepsis, and trauma. In order to elucidate vascular involvement, platelet function and platelet adhesion to traumatized endothelial surfaces will be studied. The protective effect of anti-platelet drugs will be determined. We will study the correlation between endorphins and vascular platelet adhesion and also the effects of an opiate antagonist as a potential protective agent on this process. These studies are also applicable to the changes that occur in the lung and in other organs throughout the body following shock, sepsis, and trauma. Additionally, the studies will provide valuable information in the field of vascular surgery and reconstruction.